Axonal degeneration is an active, highly controlled process that contributes to beneficial processes, such as developmental pruning, but also to neurodegeneration. In glaucoma, ocular hypertension leads to vision loss by killing the output neurons of the retina, the retinal ganglion cells (RGCs). Multiple processes have been proposed to contribute to and/or mediate axonal injury in glaucoma, including: neuroinflammation, loss of neurotrophic factors, dysregulation of the neurovascular unit, and disruption of the axonal cytoskeleton. While the inciting injury to RGCs in glaucoma is complex and potentially heterogeneous, axonal injury is ultimately thought to be the key insult that drives glaucomatous neurodegeneration. Glaucomatous neurodegeneration is a complex process, with multiple molecular signals contributing to RGC somal loss and axonal degeneration. Furthermore, the propagation of the axonal injury signal is complex, with injury triggering programs of degeneration in both the somal and axonal compartment. Further complicating this process is the involvement of multiple cell types that are known to participate in the process of axonal and neuronal degeneration after glaucomatous injury. Here, we review the axonal signaling that occurs after injury and the molecular signaling programs currently known to be important for somal and axonal degeneration after glaucoma-relevant axonal injuries.

轴突变性是一个活跃的，高度受控的过程，它有助于有益的过程，例如发育性修剪，但也会导致神经变性。在青光眼中，高眼压会通过杀死视网膜的输出神经元，视网膜神经节细胞（RGC）导致视力丧失。已经提出了多种过程来促进和/或介导青光眼的轴突损伤，包括：神经炎症，神经营养因子的丧失，神经血管单位的失调和轴突细胞骨架的破坏。尽管青光眼对RGC的诱发伤害是复杂的，并且可能是异质性的，但轴突损伤最终被认为是导致青光眼神经变性的关键损伤。青光眼神经变性是一个复杂的过程，具有多种分子信号，导致RGC体液丢失和轴突变性。此外，轴突损伤信号的传播是复杂的，在体细胞和轴突腔室中都有损伤触发变性的程序。使该过程进一步复杂化的是已知参与青光眼损伤后轴突和神经元变性过程的多种细胞类型的参与。在这里，我们回顾了在损伤后发生的轴突信号转导和目前已知对青光眼相关的轴突损伤后的体细胞和轴突变性很重要的分子信号转导程序。使该过程进一步复杂化的是已知参与青光眼损伤后轴突和神经元变性过程的多种细胞类型的参与。在这里，我们回顾了在损伤后发生的轴突信号转导和目前已知对青光眼相关的轴突损伤后的体细胞和轴突变性很重要的分子信号转导程序。使该过程进一步复杂化的是已知参与青光眼损伤后轴突和神经元变性过程的多种细胞类型的参与。在这里，我们回顾了在损伤后发生的轴突信号转导和目前已知对青光眼相关的轴突损伤后的体细胞和轴突变性很重要的分子信号转导程序。